Hippocampal Involvement With Vigabatrin-Related MRI Signal Abnormalities in Patients With Infantile Spasms: A Novel Finding.


Journal

Journal of child neurology
ISSN: 1708-8283
Titre abrégé: J Child Neurol
Pays: United States
ID NLM: 8606714

Informations de publication

Date de publication:
06 2021
Historique:
pubmed: 13 1 2021
medline: 14 1 2022
entrez: 12 1 2021
Statut: ppublish

Résumé

In a subset of infants exhibiting typical vigabatrin-related magnetic resonance imaging (MRI) changes, the authors observed additional hippocampal signal abnormalities. The authors investigated occurrence and significance of additional signal abnormalities. A retrospective review of infantile spasms patients with typical vigabatrin-related MRI abnormalities was performed. Atypical features included signal changes unilaterally or at previously unreported sites. Comparisons were made between patients with and without atypical features. In all, 26/55 (47%) exhibited typical vigabatrin-related MRI changes, with additional signal abnormalities in the hippocampi in 6 of 26. On follow-up, evolution of hippocampal signal changes paralleled changes at typical locations in 4 patients. Two patients, clinically well, without follow-up MRI. Patients with and without additional hippocampal signal changes did not differ with respect to clinical factors, including seizure status. One patient had unilateral thalamic/cerebral peduncle signal abnormality along with typical vigabatrin changes. Hippocampal changes seen in subset of patients with typical vigabatrin-related changes may be attributable to vigabatrin exposure in the appropriate circumstance.

Sections du résumé

BACKGROUND
In a subset of infants exhibiting typical vigabatrin-related magnetic resonance imaging (MRI) changes, the authors observed additional hippocampal signal abnormalities. The authors investigated occurrence and significance of additional signal abnormalities.
METHODS
A retrospective review of infantile spasms patients with typical vigabatrin-related MRI abnormalities was performed. Atypical features included signal changes unilaterally or at previously unreported sites. Comparisons were made between patients with and without atypical features.
RESULTS
In all, 26/55 (47%) exhibited typical vigabatrin-related MRI changes, with additional signal abnormalities in the hippocampi in 6 of 26. On follow-up, evolution of hippocampal signal changes paralleled changes at typical locations in 4 patients. Two patients, clinically well, without follow-up MRI. Patients with and without additional hippocampal signal changes did not differ with respect to clinical factors, including seizure status. One patient had unilateral thalamic/cerebral peduncle signal abnormality along with typical vigabatrin changes.
CONCLUSIONS
Hippocampal changes seen in subset of patients with typical vigabatrin-related changes may be attributable to vigabatrin exposure in the appropriate circumstance.

Identifiants

pubmed: 33432856
doi: 10.1177/0883073820985395
doi:

Substances chimiques

Anticonvulsants 0
Vigabatrin GR120KRT6K

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

575-582

Auteurs

Chellamani Harini (C)

Division of Epilepsy and Clinical Neurophysiology, Department of Neurology, 1862Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.

Christopher J Yuskaitis (CJ)

Division of Epilepsy and Clinical Neurophysiology, Department of Neurology, 1862Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.

Mark H Libenson (MH)

Division of Epilepsy and Clinical Neurophysiology, Department of Neurology, 1862Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.

Edward Yang (E)

Neuroradiology Division, Department of Radiology, 1862Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.

Michelle DeLeo (M)

Division of Epilepsy and Clinical Neurophysiology, Department of Neurology, 1862Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.

Bo Zhang (B)

Department of Neurology and ICCTR Biostatistics and Research Design Center, 1862Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.

Kate Mysak (K)

Division of Epilepsy and Clinical Neurophysiology, Department of Neurology, 1862Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.

Candice Marti (C)

Division of Epilepsy and Clinical Neurophysiology, Department of Neurology, 1862Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.

Jurriaan M Peters (JM)

Division of Epilepsy and Clinical Neurophysiology, Department of Neurology, 1862Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.

Ann Marie Bergin (AM)

Division of Epilepsy and Clinical Neurophysiology, Department of Neurology, 1862Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.

Phillip L Pearl (PL)

Division of Epilepsy and Clinical Neurophysiology, Department of Neurology, 1862Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.

Sanjay P Prabhu (SP)

Neuroradiology Division, Department of Radiology, 1862Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.

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Classifications MeSH